ABSTRACT
The basic driving unit of oscillatory electrical activity in stomach and intestine is the slow wave, a propagating depolarization of myogenic origin. The slow wave controls contractile activity in the intestine by triggering action potential bursts, while in the stomach there is both action potential and spike-free slow wave activation. This review attempts to summarize recent characterizations of the slow wave and to explore in detail the evidence, which suggests that the mechanisms which generate the electrical oscillations are quite closely coupled to metabolic processes.
To illustrate this, one can estimate the charge movements in a small sphere 5 in diameter bounded by a membrane having the specific resistance of taenia coli, 50000 Ω cm2 (Abe & Tomita, 1968). Since the membrane time constant of intestinal muscle measured under space-clamped conditions is roughly the same as that of taenia coli this is a reasonable value to choose. The resting value of free internal calcium is conservatively estimated at 10−7 M (Dipolo et al. 1976). To cause a steady transmembrane voltage change of 1 mV, an insignificant quantity with respect to normal measurement capabilities, would require a current of 1·6 × 10−14 A, which if carried by Ca2+ would be an influx of 0·83 × 10−14mol/sec. This influx would increase the total calcium concentration of the sphere by 1·3 × 10−6 M per second or over 10 × the free calcium level. Of course only a fraction of the influx would appear as the free ion since intracellular calcium is strongly buffered but since the membrane is the site of entry, the free calcium concentration would be greatest near the membrane inner surface. The characteristics of calcium buffering, transport and distribution are not well enough understood at this time to extend this illustration further than the point that small calcium fluxes and changes in the fluxes, while being without much direct effect on electrogenesis may have significant effects on internal concentration of the free ion.
